Nerve growth factor acts with the beta2-adrenoceptor to induce spontaneous nociceptive behavior during temporomandibular joint inflammatory hyperalgesia.
OBJECTIVE
The aim of this study was to investigate whether the injection of nerve growth factor induces spontaneous nociceptive behavior in the intact or sensitized temporomandibular joint (TMJ) of rats.


METHODS
NGF was injected into the TMJ 1 h after the TMJ injection of saline or carrageenan and the spontaneous nociceptive behavior was quantified. The mechanism involved in this phenomenon was investigated by the injection of NGF into the carrageenan-sensitized TMJ in the presence of indomethacin or of beta-adrenergic antagonists.


RESULTS
NGF injected into the TMJ sensitized by a prior TMJ injection of carrageenan but not into the intact TMJ induced a significant nociceptive behavior. Co-injection of the non-specific Trk receptor antagonist k252A with NGF 1 h after the TMJ injection of carrageenan significantly reduced NGF-induced spontaneous nociception supporting the Trk receptor activation in this nociceptive effect. Blockade of prostaglandin synthesis by indomethacin before the TMJ injection of carrageenan did not reduce NGF-induced nociception. Co-administration of carrageenan with the beta2-adrenoceptor antagonist ICI 118.55 but not with the beta1-adrenoceptor antagonist atenolol significantly reduced NGF-induced nociception. The injection of NGF the TMJ sensitized by a previous TMJ injection of epinephrine also induced nociceptive behavior.


CONCLUSIONS
Taken together, these results indicate that NGF can induce TMJ nociception during TMJ inflammation. Moreover, the expression of this nociceptive response seems to depend on the synergic activity of NGF and sympathetic amines released during TMJ inflammation acting on beta2-adrenergic receptors.
Pelegrini-da-Silva
Adriana
A
Department of Physiological Sciences, Laboratory of Orofacial Pain, Piracicaba Dental School, University of Campinas-Piracicaba, São Paulo, Brazil. adriana-ps@bol.com.br
Oliveira
Maria Cláudia G
MC
Parada
Carlos Amílcar
CA
Tambeli
Cláudia Herrera
CH
D058672:Adrenergic beta-2 Receptor Antagonists; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D002227:Carbazoles / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D006930:Hyperalgesia / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D026121:Indole Alkaloids / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D020932:Nerve Growth Factor / Q000494:pharmacology / Q000502:physiology*; D009619:Nociceptors / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020917:Receptor, trkA / Q000037:antagonists & inhibitors; D018343:Receptors, Adrenergic, beta-2 / Q000502:physiology*; D013705:Temporomandibular Joint Disorders / Q000150:complications / Q000378:metabolism / Q000503:physiopathology
D058672:Adrenergic beta-2 Receptor Antagonists; D002227:Carbazoles; D004791:Enzyme Inhibitors; D026121:Indole Alkaloids; D011453:Prostaglandins; D018343:Receptors, Adrenergic, beta-2; D020932:Nerve Growth Factor; C049985:staurosporine aglycone; D020917:Receptor, trkA; D007213:Indomethacin; D004837:Epinephrine